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==Well, honestly YOU led the thread in all sorts of OT direction. And, now, simply b/c you don't have your usual SMUG "BIOLOGY EXPERT"  response, you want claim hijacking?? Really?!!  YOU ARE A TYPICA

You sample an early patient. You sample a later patient. You compare them. You see how much it’s mutated. You do the same for flu.  You see if covid mutates as quickly as flu. How is this a question f

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1 hour ago, invasive-feces said:

On another note, might deliberately co-infecting the COVID-19 patient with another virus (say common cold) help somehow with build up of COVID-19  antibodies? Has anything like this been investigated?

Basically that would not work. Adaptive responses react to specific antigen presented by a given causative agent of disease. The only possible scenario would be e.g. another coronavirus that has an antigen that is very similar to one from SARS-CoV-2. But that would be highly unlikely as a whole.

Also co-infection is a bad idea, immunity (if it happens) is built during later stages of the response. Theoretically having multiple diseases is not a good situation especially if they can make things worse for the patient. 

I.e. you would want the immunization happen before getting the disease (which is the idea of vaccines and why vaccines cannot be used as a treatmen).

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Is there any potential for a lozenge, spray or mist that could coat the throat and upper airway in such a way as to reduce the spreading of the virus by an infected patient? Particularly asymptomatic ones...the thought being that without the coughing/wheezing etc they should be low transmitters but are said to be otherwise, for some reason that has yet to become clear (I've heard they have a higher viral count, if that is the correct term)

Is there anything that could act as a barrier to any degree, that would not be detrimental to the user?

Or even something that could act to reduce the viral count in the surfaces of the upper airway (which presumably could reduce the amount of virus exhaled)

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Another co-factor to investigate would be seasonal flu shot vs. COVID-19 deaths (or serious CV19 cases). That is, might a seasonal flu -- even a very MILD case -- weaken  one's defenses to "allow" SARS-COv-2 to "get in" and/or become aggressive?

Edited by invasive-feces
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On 5/5/2020 at 4:42 PM, CharonY said:

I suspect the question is aimed at respiratory disease. I believe it has been asked and answered a few times, though knowledge is of course evolving. There are handful of studies who have tested COVID-19 positive patients for e.g. influenza, other coronaviruses an so on. In one study from Wuhan the co-infection rate was about 20%. In other regions such as Italy I have seen some higher estimates but with fewer tests.

 ~20%

https://www.cidrap.umn.edu/news-perspective/2020/04/researchers-report-21-covid-19-co-infection-rate

https://med.stanford.edu/news/all-news/2020/03/covid-19-can-coexist-with-other-respiratory-viruses.html

https://wwwnc.cdc.gov/eid/article/26/6/20-0299_article

 

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14 hours ago, invasive-feces said:

Another co-factor to investigate would be seasonal flu shot vs. COVID-19 deaths (or serious CV19 cases). That is, might a seasonal flu -- even a very MILD case -- weaken  one's defenses to "allow" SARS-COv-2 to "get in" and/or become aggressive?

I vaguely remember that someone was looking into outcomes of folks with seasonal influenza co-infection but I just cannot remember the author. The only thing that I took away is that there was no indication that co-infections had a significant impact on outcome per se. Once the cases become severe, however complications from other infections become more problematic. That being said, I doubt that we have enough information to have definite answers- many of these studies were small in scale and quickly published (for obvious reasons) so conclusion may change once new findings pop up rather rapidly. 

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@CharonY @Arete or anyone else who feels competent, could you folks please translate the below paper to non PhD for me? I understand the abstract and the introduction but the rest is too much for me. Are these anti bodies something parallel to vaccine research or something else like they claim, what are the implications?:

https://www.nature.com/articles/s41467-020-16256-y

Edited by koti
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In short, they identified a singular (monoclonal) antibody that binds to a conserved area in coronaviruses and found that if it binds, it interrupts the ability of the viruses to invade cells.

It is at this point more a mechanical/functional study showing that presence of antibodies could at least fundamentally disrupt invasion by viruses. This gives hope to convalescent serum treatment for example. Of course it is not ensured that folks producing antibodies (they are always a mix, or polyclonal) will develop something similar. 

It is unlikely to influence vaccination development much I think, most target the spike protein anyway. It does increase the likelihood that immunization is feasible though (I think).

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Anyone know how many of the positive (tested) CONFIRMED cases were/are asymptomatic?

E.g., as of today, according to 

https://ncov2019.live/

...in the U.S.A, there are:

1,384,033

How many are just " confirmed asymptomatic"?

 

According to..

https://www.ecdc.europa.eu/en/case-definition-and-european-surveillance-human-infection-novel-coronavirus-2019-ncov

European Centre for Disease Prevention and Control--An agency of the European Union

Confirmed case 
A person with laboratory confirmation of virus causing COVID-19 infection, irrespective of clinical signs and symptoms 

Not sure how many countries follow THAT definition.

Edited by invasive-feces
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34 minutes ago, invasive-feces said:

Anyone know how many of the positive (tested) CONFIRMED cases were/are asymptomatic?

It seems pretty uncertain at the moment. Somewhere between 0 and 100%

For example:

Quote

 between 5% and 80% of people testing positive for SARS-CoV-2 may be asymptomatic

https://www.cebm.net/covid-19/covid-19-what-proportion-are-asymptomatic/

Quote

A total of 130 of 166 new infections (78%) identified in the 24 hours to the afternoon of Wednesday 1 April were asymptomatic

https://www.bmj.com/content/369/bmj.m1375

Quote

2.2 percent of NZ Covid-19 cases asymptomatic

https://www.newsroom.co.nz/2020/05/09/1161521/22-of-new-zealand-covid-19-cases-asymptomatic

Quote

ion of infections, along with the infections’ timeline. The estimated asymp- tomatic proportion was 17.9%

http://med.stanford.edu/content/dam/sm/id/documents/COVID/AsymptCOVID_TransmissionShip.pdf

 

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The data are also only partially help to establish that. In almost all countries tests are administered after indication, which could include symptoms but also e.g. contact with positive persons. In conjunction with the fact that a positive person may exhibit not symptoms the data will mostly show bias in sampling procedure or of the cohort.

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I going to guess -- prove otherwise-- that most of the cases reported (recorded) are more from "dragnetting" operations as opposed to emergency-room walk-ins.

In other words, some one on a cruise ship, nursing home, etc. gets sick and is confirmed positive for COVID-19. And that leads to testing of that person's contacts and community. And many of those will test +, but be/remain asymp.

 

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It highly depends on how the respective health authorities collect their data. Some do not actually record symptoms and only provide hospitalizations rates, for example. Also note that you can asymptomatic when tested, but develop symptoms after. Recording these things accurately is difficult unless you have identifiers for each person (which is generally not the case).

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I'm not sure much definitive info exits on COVID-19's "endemicness" in the open population.

That is, how long does this virus remain remain transmissible in any given individual (whether or not they became symptomatic)?

Can this virus "hide out" in an individual's system ... even for life (as in the case for herpes)?

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It is not 100% understood. Indirect (i.e. epidemiological data) suggest highest likelihood during symptomatic periods and it appears that respiratory titer go down or vanish after symptoms are gone (or  ~10- days after onset of illness in mild cases). 

Shedding e.g. by feces seem to go on for longer, but it is not clear whether those are a source of infections. I do not think anything is known about potential of persistence at this point. 

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1 hour ago, invasive-feces said:

I just heard a report on Science Friday (??) that COVID-19 was found in semen. So it may be (or have become) sexually communicable. 

https://www.webmd.com/lung/news/20200507/virus-found-in-semen-of-covid-19-survivors

Obviously that would be a concern, but if we can assume it can be sexually transmitted, let's say vaginally, would that give the body more time to adapt than breathing in the virus, given that this manifests most dangerously as a respiratory disease?

Broadening the question what is generally the most dangerous way to "catch" a flu or flu like disease?

Not to be confused with most likely way to "catch" it. Is there a way to get it that is least/most preferred, assuming you would get it? 

I did see some claim that abstinence was advised for 28 days after recovery as a precautionary measure.

Edited by J.C.MacSwell
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About shedding and its temporality .... this Nature Medicine paper, about a month old now,   seems to indicate Wuhan median = 20 days (max 37)

Temporal dynamics in viral shedding and transmissibility of COVID-19

https://www.nature.com/articles/s41591-020-0869-5

 

45 minutes ago, J.C.MacSwell said:

Obviously that would be a concern, but if we can assume it can be sexually transmitted, let's say vaginally, would that give the body more time to adapt than breathing in the virus, given that this manifests most dangerously as a respiratory disease?

 

Introduce the word "sex" and it's like ringing the dinner for the media!

But the added sensational spotlight may not be such bad thing it prompts more research $$$ into medical SCIENCE ;)

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It is rather unlikely that it is a significant path. First of all, respiratory droplets are (hopefully) deposited much more frequently and broader than semen fluids. Second, I do not think that the receptor is found in significant abundance in female tissue. 

1 hour ago, J.C.MacSwell said:

Obviously that would be a concern, but if we can assume it can be sexually transmitted, let's say vaginally, would that give the body more time to adapt than breathing in the virus, given that this manifests most dangerously as a respiratory disease?

Now, as mentioned, vaginal tissue does not seem a likely target of the virus. However there are than the lung. One of them, the kidney is also a target and in some patients renal failure has been reported. That is obviously not good either.

However, ACE2 receptors are found in the gastrointestinal tract. There is at least one guy who has speculated that potentially infecting folks through the GI tract might be a way to induce immunity with potentially less harmful symptoms. However, ultimately we know to little about the pathophysiology to make any calls at this point. But there is more research looking at GI infections now.

As a minor point: note how fast research has been moving (relatively speaking). Beginning of the year we weren't sure what we were dealing with at all, now folks are exploring things on a rather broad front.

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It may act as a systemic inflammatory agent.
Other than the respiratory tract, GI tract and kidneys, it also seems to inflame blood vessels, leading to a thickening ( gelling ? ) of blood.

There is also the systemic inflammation that has been affecting children, and linked to Covid-19.

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16 minutes ago, MigL said:

It may act as a systemic inflammatory agent.
Other than the respiratory tract, GI tract and kidneys, it also seems to inflame blood vessels, leading to a thickening ( gelling ? ) of blood.

There is also the systemic inflammation that has been affecting children, and linked to Covid-19.

My oldest son had Kawasaki's disease. As far as I know there is no increased risk as he full recovered around 20 years ago.

Coincidentally he is at the house today for the first time in over two months after yesterday's easing of restrictions in Nova Scotia.

Edited by J.C.MacSwell
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Having had Kawasaki does not put you at higher risk.
But this affliction, very similar to Kawasaki, has been linked ( in UK, Italy and US ) to Covid-19

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1 minute ago, MigL said:

Having had Kawasaki does not put you at higher risk.
But this affliction, very similar to Kawasaki, has been linked ( in UK, Italy and US ) to Covid-19

I saw that. As far as I know Kawasaki's is a set of symptoms of unknown cause, so maybe the Covid virus manifests that way in some children?

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